EC5026 is a fatty acid amide hydrolase (FAAH) inhibitor being developed by EicOsis for the treatment of Parkinson's disease. The STEP Study (NCT07142044) is a Phase 1 clinical trial evaluating the safety, tolerability, and pharmacokinetics of EC5026 in patients with Parkinson's disease["eicosis2024"].
FAAH inhibition represents a novel approach to Parkinson's disease therapy by modulating the endocannabinoid system, which plays important roles in neuroprotection, neuroinflammation, and motor control["faahpd"].
Trial Details
Key Information
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Overview
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EC5026 is a fatty acid amide hydrolase (FAAH) inhibitor being developed by EicOsis for the treatment of Parkinson's disease. The STEP Study (NCT07142044) is a Phase 1 clinical trial evaluating the safety, tolerability, and pharmacokinetics of EC5026 in patients with Parkinson's disease["eicosis2024"].
FAAH inhibition represents a novel approach to Parkinson's disease therapy by modulating the endocannabinoid system, which plays important roles in neuroprotection, neuroinflammation, and motor control["faahpd"].
The trial employs a randomized, double-blind, placebo-controlled design:
Allocation: Randomized (escalating dose cohorts)
Intervention: EC5026 oral tablets
Control: Matching placebo tablets
Duration: Multiple ascending dose (MAD) cohorts
Follow-up: 4-week safety follow-up
Mechanism of Action
FAAH Inhibition
Fatty acid amide hydrolase (FAAH) is the primary enzyme responsible for degrading endogenous cannabinoids (endocannabinoids) such as anandamide. By inhibiting FAAH, EC5026 increases anandamide levels in the brain, which:
Reduces Neuroinflammation: Endocannabinoid signaling modulates microglial activation and reduces inflammatory cytokine production
Provides Antioxidant Effects: Anandamide exhibits antioxidant properties that may protect dopaminergic neurons
Modulates Motor Control: The endocannabinoid system influences basal ganglia function and motor coordination
Therapeutic Rationale
Parkinson's disease involves progressive degeneration of dopaminergic neurons in the substantia nigra, leading to motor symptoms. FAAH inhibition may address multiple aspects of PD pathophysiology:
Neuroprotection: Enhanced endocannabinoid signaling may protect remaining dopaminergic neurons from degeneration
Anti-inflammatory Effects: Reduced neuroinflammation could slow disease progression
Motor Symptom Modulation: CB1 receptor modulation may improve motor function
This mechanism differs from conventional dopamine replacement therapies by targeting the underlying disease process rather than just symptoms.
Inclusion Criteria
Age 40-75 years
Diagnosis of idiopathic Parkinson's disease (UK Brain Bank criteria)
Disease duration 1-15 years
Hoehn & Yahr stage 1-3
On stable PD medication regimen for ≥4 weeks (if receiving treatment)
MDS-UPDRS Part 3 score ≥10
MMSE score ≥24
Able to swallow tablets
Willing to comply with study procedures
Written informed consent
Exclusion Criteria
Atypical parkinsonism (PSP, MSA, CBS)
Significant cognitive impairment (MMSE <24)
History of stroke or significant neurological disease
Active malignancy
Severe medical conditions (cardiovascular, hepatic, renal)
Prior FAAH inhibitor therapy
Known hypersensitivity to EC5026
Pregnancy or breastfeeding
Current participation in other clinical trials
Substance abuse disorder
Endpoints
Primary Endpoints
Safety and Tolerability: Incidence and severity of adverse events
Pharmacokinetics: Cmax, AUC, half-life of EC5026
Secondary Endpoints
Pharmacodynamics: Changes in anandamide levels
MDS-UPDRS Parts 1-3 (motor and non-motor scores)
PDQ-39 (quality of life)
MoCA (Montreal Cognitive Assessment)
Exploratory Endpoints
Biomarker analysis (inflammatory markers)
CSF sampling (in selected cohorts)
Neuroimaging substudy
Study Population
Target Population
Early to mid-stage Parkinson's disease patients who:
Meet clinical diagnostic criteria for idiopathic PD
Have no significant comorbidities
Are able to complete all study assessments
Sample Size
The Phase 1 trial will enroll approximately 40-60 healthy volunteers and PD patients across multiple dose escalation cohorts.
Safety Profile
Expected Profile
Based on preclinical data and known FAAH inhibitor class effects: